Histoplasmosis et cetera Page

The dangers, including the biohazards, need to be taught
throughout the caving community. The medical profession needs instruction.
However the dangers need to be kept in perspective.

By far the most common Lung Fungus which cavers need to be
concerned with is Histoplasmosis. Most doctors are not familiar with
Histoplasmosis or the other lung fungi described here. Cavers developing
respiratory problems from several days to several weeks following caving trips
should consult their doctor and tell them that they are cavers and that Histo is
suspected. In some cases cavers may need to educate the doctor about what Histo
is. Copies of the items on this page may be found useful by the treating
physician.

Direct link to our other Biohazards Pages

Send
us your additions or comments about the above information. We want to be as
complete and accurate as possible.

Much of this information is excerpted from email postings and is
not necessarily the complete or edited versions that the individual author would
submit as a professional paper and should be considered as being presented for
informational purposes only. Readers are cautioned to not read too much into any
statement and to please not be too critical of grammar or spelling. I have done
some minor editing to aid clarity or word flow. Usually I did nothing. --Ediger

I'm not an MD, but I have followed this subject ... in the
scientific literature for years.

The risk of histo is pretty good if you go caving in Texas,
Mexico and parts south, especially if you are new to caving or from non-endemic
areas (NE USA, Canada, Europe).

One can never get perfect immunity to histo. Many cavers and
guano miners develop good resistance to it, but the lungs just wall off the
infections in little cysts in the lung. One can get histo, even if you have been
exposed before, and I have seen this happen even in experienced cavers. All it
takes is getting a big dose of spores, or having your immune system down a bit,
and so on.

Many cavers in Texas, the South, and Mexico have high resistance
to histo. It is usually novices, and cavers from the northeastern US, Canada,
and Europe who are vulnerable. There was a small outbreak in a caving group
(mostly novices, I heard) from Houston, TX, about 10 years ago. They had visited
Beck Ranch Cave near Round Rock. At that time I worked for the Texas Dept. of
Health, and I was sent to the cave to do air and soil sampling for histo. We had
a special viable microbial air sampler. After testing several areas, we found
Histoplasma spores only in the bat roost, where Myotis
velifer guano is found.

We still don't know if a guano miner, who usually would mine
Mexican free-tailed bat guano, would be likely to get histo, but I guess it's
possible. It just seems that in Texas it's more likely in Myotis
velifer caves. But Histoplasma is found in all kinds of bat and bird
guano. Cleaning up pigeon roosts has caused a lot of occupational cases of
histo. I know one Brit who got a histo infection in his eye in a cave in Belize.
He eventually lost that eye.

Another letter from William R. Elliott, PhD excerpted
from CaveTex message Monday 19 April 1999

When I lived in the lower Rio Grande Valley from 1977-1981,
there was an outbreak of histo among some cavers from McAllen who went to
Carrizal. I collected health questionnaires from them to see if there was any
pattern. I will have to look in my old files and see if I still have the data.
Most of the group who went got histo, and several were diagnosed with it and
treated, but not all were sick or clearly diagnosed. One problem with histo is
that the blood test can give the dr. a false negative if it is done too soon. It
may be better to wait until a month after exposure (about two weeks after
symptoms start). Of course, one wants to know right away and get the proper drug
(itroconazole is the drug of choice right now). Getting diagnosed and treated
properly is pretty hit and miss.

One thing I want to caution cavers about is that you don't have
to walk through a dry, dusty guano area to get histo. I know people who have
gotten histo from rather damp caves. After the histo outbreak in 1994 from the
NSS Convention, the CDC did a number of studies and found no histo in Mexican
freetail guano, but did find it in Myotis velifer (cave myotis) guano. The
latter tends to be more moist, but we do not know if that is the only factor in
getting the fungus to grow. By the way, the visible fungus growing on guano is
not Histoplasma. Histoplasma fungus is microscopic, and you cannot
see it on the guano.

It would be interesting if someone were to study the year-round
bat usage of Gruta de Carrizal, and see which species and what parts of the cave
are involved. But it looks like most parts of the cave are involved. Perhaps it
has to do with migrating Myotis velifer, some of which may overwinter in Mexico
but move back to Texas in the spring. We don't know where all the Myotis velifer
go in the winter. Some may hibernate in Northwest Texas caves. Then they're back
in force in Central Texas caves in spring and summer. The histo cases I know of
personally from Texas involved Myotis velifer caves.

5 years ago, I visited a pulmonologist at the Baylor College of
Medicine and he prescribed to me the following medication:

Commercial name: Sporanox

Formula name: Itraconazole.

I was told that several of the -azole medications would probably
treat histo. After a week on this medication my cough went away. Histo may show
up on your chest x-rays. The picture may look like you have white peas growing
in your lungs. In my case, there was about one per square inch. I never did get
a x-ray after I got well. But a recent x-ray didn't show anything unusual.

By the way, I have been in Grutas de Carrizal about 15 times. I
don't know if I have ever caught histo in this cave. I used to cough a lot and I
always thought it was due to bronchitis. In my opinion, anyone susceptible to
respiratory illnesses, such as bronchitis should avoid caves with large bat
colonies. If you visit a cave with a large bat colony and two weeks later, get a
cough that causes you discomfort, you should immediately go to see a
pulmonologist.

IMPORTANT NOTE:
This work is over 20 years old and some of the information regarding treatment
is out-of-date. Do not rely on it for accuracy when looking for or prescribing
treatment.

HISTOPLASMOSIS

Histo is a highly infectious pulmonary or disseminating disease caused by the
fungus Histoplasma capsulatum. The disease occurs throughout the world
and is especially prevalent in northeast, central, and south central United
States. It is found as a saprophyte in the soil, and man and animals contract it
by inhaling the infectious spores. Most Histo epidemics reported involved
persons who had been exposed to the fungus in a cave, silo, storm cellar, or
chicken house.

Histoplasmosis is primarily a pulmonary (lung) infection, but it
can range from a benign self-limiting type to a chronic disseminating type. Some
cases are sub-clinical and show no symptoms at all; the disease is evidenced
only by a positive histoplasmin skin test. In a more serious form, histo is
accompanied by fever, malaise, cough, and loss of weight. Meanwhile, the lungs
are filling with lesions which either undergo re-solution, or calcify in 4 to 5
years. This gives the lungs a pebble beach appearance on an x-ray. If one's
really unlucky, the pulmonary histo can disseminate. This means that the fungus
leaves the lungs via the lymph or circulatory systems and heads out to
parasitize other systems. The spleen is a favorite target and may he calcified
which wreaks havoc on the erythrocytic breakdown rate and results in an
enlarged, hard spleen. The liver can be hit and this means hassles for the
body's major cleanup and digestive organ. Secondary anemias and decreased white
cell counts also occur, meaning general tiredness and susceptibility to
infection. The patient is also hit with fever, sweats, and becomes emaciated.
Mucocutaneous lesions of the skin, tongue, pharynx, and larynx can appear and
then ulcerate, which results in loss of tissue and cellular structures.

H. capsulatum is a biphasic fungus (a fungus in living
tissue, a yeast on non-living media). On blood agar plates at 3700, the organism
exhibits a smooth, cream to white colony. Microscopally, it is composed of small
oval single budding cells with branching septate hyphae. The spores of H.
capsulatum are characteristic and therefore diagnostic. The spore, a
chlamidospore, is covered with fingerlike projections, and is known as a
'tuberculated chlamido spore'.

Most cavers are histoplasmin positive. This means that most
cavers have been sufficiently exposed to H. capsutatum
specific antigen that said antigen has triggered an immune response and the
caver has built up antibodies to the disease. Back in 1958, Heiner was able,
through gel diffusion techniques, to isolate the six antigens basic to H.
capsulatum. In 1960, Greene purified the 'h' and 'rn' antigens, isolated
them, and came up with the first histoplasmin. The histoplasmin skin test works
like this: histoplasmin (the antigen), when injected into the skin of a person
with antibodies to histoplasmosis (these antibodies having been made in response
to exposure to H. capsulatum) reacts with said antibodies to cause a
reddening of the skin. This constitutes a positive test and can indicate
anything from exposure only to disseminated Histo, AnAgglutination Test and a
Fluorescent Antibody Technique are also available.

If you come up histoplasmin positive and pulmonary symptoms are
present, further tests are done. Blood, sputum, and possibly bone marrow is
collected and stained for the presence of polymorphonUclear cells. It should
also be cultured on BHI media in order to isolate H. capsulatum. If these
stains and cultures indicate Histo, then the problems of treatment begin. Many
drugs and antibiotics have been used without success; at this time Amphotercin B
is the drug of choice as it is the most effective with the least number of
unfavorable side-effects.

There is, at this time, no vaccine against Histo, although the
body does a pretty good job of limiting infection to a subclinical level through
its own antibody buildup and immunization system.

1999 Note: Coccidiomycosis is not a cave fungus. It is a
heat-loving, desert fungus spread by inhaling infected dust. Diggers near
surface areas in caves have been infected. The danger to cave explorers who do
not dig is remote. It is presented here for information purposes only to
accompany the discussion on Lung Fungi and to dispel rumors.

Coccidiodes immitus is a fungus that produces the highly
infectious disease of Coccidiomycosis or San Joaquin Fever. The severity of
infection can range from a benign, self-limiting respiratory infection to a
malignant disseminating form known as Coccidiodal Granuloma. The disease is a
dustborne one, native to the arid regions of the US (namely California, Arizona,
New Mexico, and West Texas) and Mexico. Inhabitants of these areas are usually
coccidiodin-positive. The disease is acquired upon inhaling spore-laden dust.

Coccidiomycosis is usually self-limiting in the white-skinned
race, but has a tendency to develop into the malignant form in dark-skinned
people. The benign primary infection can be subclinical or, after an 8 to 14 day
day incubation period, cause 'flu'-like symptoms. These include chills, fever,
cough, pleurisy, body aches, and night sweats. Some 2 to 5% of these cases
develop an allergic response characterized by raised reddened areas (erythema)
and skin lesions. This form of coccidiomycosis is known as San Joaquin or Valley
Fever. The prognosis for these benign forms is excellent. Enforced bed rest is
imperative and the disease is treated symptomatically until temperature and
white cell count are normal.

The malignant disseminated Coccidiodal Granuloma is a different
story. The symptoms are tike those of tuberculosis lesions and appear in the
lungs as well as the larynx, lymph nodes, bones, joints, and central nervous
system. These lesions can be so severe in the lungs that surgery and resection
is often required. Coccidiodal Granuloma is often fatal but Amphotercin B, the
drug of choice, has been used successfully. C. immitus is a filamentous
fungus. It can be grown on all common lab media with SAB being the media of
choice. On SAB a rapid-growing white, cottony colony that turns brown and
powdery with age is Characteristic of the fungus; microscopically, the hyphae
look tike string beans, the 'beans' being the characteristic arthrospores
diagnostic of coccidiomycosis. In the living tissues of a host the diagnostic
structure is known as a 'spherule'. This is a large, thick-walled bag that is
fitted with smaller endospores. These endospores are the infectious stage of the
disease when they become airborne or dust-borne.

Coccidiodin is the purified specific antigen of C. immitus.
When it is injected into the epidermis of a person with antibodies to
coccidiomycosis (produced in response to an earlier exposure) a reddening area
occurs. This constitutes a positive test that can indicate anything from simple
exposure to Coccidiodal Granuloma. In persons with the latter however, other
antibodies are present; these include complement fixing antibodies and
precepitins. The presence of complement fixing antibodies (these cause blood
cell lysis or destruction) in high titers indicates a spreading infection and a
poor prognosis. A test for the precipitin antibody is positive only after very
recent infection. Recovery from any form of coccidiomycosis imparts a lasting
immunity to the person; this means that if one is coccidiocin-positive and has
no symptoms of the disease, he is very probably immune for life.

In the presence of a positive coccidiodin and symptoms of the
disease further tests must be done. Pus, sputum, gastric washings, and/or
pleural fluid should be microscopically examined for endospore-filled spherules
as well as cultured for characteristic colony morphology of C. immitus.
In cases of Coccidiomycosis, symptomatic treatment, rest, and Amphotercin B are
the best treatment.

1999 Note: We do not know of a single case of
blastomycosis in a caver. The only Blasto case was reported by a caving
expedition to Costa Rica. That identification has not been confirmed to be cave
related

Blastomyces dermatitidis is a yeastlike fungus which
causes North American blastomycosis or Gilchrist's Disease. The disease can
occur as a primary pulmonary self-limiting disease similar to Histoplasmosis,
Coccidiomycosis, and Tuberculosis.

Blasto is a chronic granulomatous infection of the skin and
internal organs. In rare cases it exhibits itself as a primary cutaneous
infection in which lesions of the skin appear with lymphatic involvement. The
lesions start as blister-like papulopustules which spread outward from a
granulomatous base that is covered with a dirty pink exudate. When these lesions
heal, they leave a paper thin scar tissue surrounded by a raised edge.

Primary pulmonary btastomycosis can be mild with only minor lung
congestion as in a bad cold, or severe enough to mimic tuberculosis or lung
cancers. If B. dermatitidis leaves the lung via the circulatory system
then skin, subcutaneous tissue, and even the bones often become involved. They
are all subject to gumma-like lesions which burst spontaneously releasing a
bloody pus. The liver, spleen, kidney, and central nervous system are also
subject to the lesions to a lesser extent. Under microscopic examination, the
lesions contain polymorphonuclear cells, cell debris, and giant cells, and
sometimes the fungus itself.

There is only one antigenic type of B. derrnatidis, but
the antibody that the human body builds up can cross react with B.
dermatitidis as well as Histoplasma capsulaturn
and Candida albicans. The Fluorescent Antibody Technique is the best
method of demonstrating the presence of B. dermatitidis. Complement
Fixation Tests can demonstrate the antibodies in patients with extensive or
progressive infection which indicates a poor prognosis, but those patients with
only localized cutaneous lesion test negative for Blastomycosis. Just to
complicate things further, a skin test for Blasto gives a reddened raised area
at the injection site in cases of actual
B. dermatitidis infection as well as Histo and Coccidio. The disease is
therefore difficult\ to diagnose easily.

About the best way to diagnose Blastomycosis is to examine
lesion crusts, sputum, pus, urine, and/or spinal fluid for the presence of B.
dermititidis fungus. The fungus appears as a thick-walled, single budding
yeast-like organism. If specimens containing the organism are grown on Blood
agar or SAD agar at 37C colonies that look like disembodied brains grow. Under
the mictoscope the myceleal stage is composed of short, broad 3 to 4 celled
hyphal segments with budding yeast-like cells. After a time the brain appearance
of the colony is completely covered over by a white cottony mycelial mat.

Most patients infected with B. dermatitidis
live in the Eastern section of the US and North American Blastomycosis is
completely, without exception, limited to the US and Canada.. Patients suffering
from the infection should be treated supportively with high-vitamin,
high-calorie diets and prolonged bed rest. The drugs stilbamide and
dihydroxystibamidine have been used with some success for both cutaneous and
systemic blastomycosis. Those infections which proved resistant were usually
successfully controlled with Amphitericin B. In very severe cases, pulmonary
resections and lobectomies have been performed with some success.

IMPORTANT NOTE:
This work is over 20 years old and some of the information regarding
treatment is out-of-date. Do not rely on it for accuracy when looking for or
prescribing treatment.